The "dependent viscera" sign in CT diagnosis of blunt traumatic diaphragmatic rupture

OBJECTIVE: The objective of our study was to describe the "dependent viscera" sign and determine its usefulness at CT in the diagnosis of diaphragmatic rupture after blunt abdominal trauma. MATERIALS AND METHODS: The study sample consisted of 28 consecutive patients (19 men, nine women) between 17 and 74 years old (mean age, 31 years) who had undergone abdominal CT and subsequent emergency laparotomy after a blunt trauma. Ten patients had a diaphragmatic rupture (six, right-sided; four, left-sided) at laparotomy. An experienced radiologist unaware of the surgical findings retrospectively reviewed the CT scans, and then a second radiologist reviewed the scans to provide interobserver agreement. Note was made of discontinuity of the diaphragm, intrathoracic herniation of abdominal contents, and waistlike constriction of bowel (the collar sign). Also noted was whether the upper one third of the liver abutted the posterior right ribs or whether the bowel or stomach lay in contact with the posterior left ribs. Either of these findings was termed the "dependent viscera" sign. The radiologists' detection rate of diaphragmatic rupture on the CT scans via observance of the dependent viscera sign was determined. Interobserver agreement was assessed using Cohen's kappa statistic. RESULTS: The dependent viscera sign was observed on the CT scans of 100% of the patients with a left-sided diaphragmatic rupture and of 83% of the patients with right-sided diaphragmatic rupture. Both observers missed one case of right-sided diaphragmatic rupture. The radiologists' overall rate of detecting diaphragmatic rupture was 90% using the dependent viscera sign. We found excellent interobserver agreement (kappa = 1) for detection of the dependent viscera sign and for the diagnosis of diaphragmatic tear on CT scans. CONCLUSION: The dependent viscera sign increases the detection at CT of acute diaphragmatic rupture after blunt trauma.     

Blood-brain barrier sodium transport limits development of brain edema during partial ischemia in gerbils

Sodium derived from the blood is known to accumulate in brain tissue during the early stages of incomplete ischemia. Our present studies were undertaken to determine the relation between blood-brain barrier sodium transport and the development of ischemic brain edema. Incomplete cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. Following recovery from the anesthetic, the gerbis were evaluated for the presence of neurologic symptoms and were divided into symptomatic (n = 77) and asymptomatic (n = 94) groups. Tissue water, sodium, and potassium contents, tissue plasma volume, and brain uptake of 22Na were measured in both groups 1.5, 3, 6, 12, and 24 hours after carotid ligation. There was a progressive accumulation of sodium and water in the ipsilateral cerebral cortex of the symptomatic group compared with either the corresponding contralateral cortex of the same gerbils or with the asymptomatic group. Net changes in brain sodium and potassium concentrations appeared to be the main determinants of fluid accumulation. Brain edema was not due to opening of the blood-brain barrier because the unidirectional transport of 22Na remained low and was even reduced by 35-55% in the ischemic cortex. Nevertheless, this sodium transport activity appeared to be rate-limiting in the development of brain edema during the first 3 hours of ischemia because the rate of sodium accumulation in the tissue was the same as the rate of 22Na transport from the blood to the brain. We conclude that blood-brain barrier sodium transport is an important factor in the formation of ischemic brain edema.     

Abdominal computed tomography in patients with small cell lung cancer

The results of abdominal computed tomography in 38 patients with small cell lung cancer are reported. 47% patients had abnormal scans. Liver metastases were present in 24%, adrenal enlargement in 24% and lymphadenopathy in 8%. Two of the three patients (8%) with bilateral adrenal enlargement had ectopic hormone production. Overall 11% patients with retroperitoneal metastases had their staging changed from limited to extensive disease due to computed tomography.     

Accuracy of blood glucose measurements using a reflectance meter.

The performance of a stock reflectance meter for measuring blood glucose levels with glucose oxidase test strips has been assessed. Glucose values obtained were spuriously high, and the response of the instrument was non-linear. The instrument could not be recommended as an accurate means of determining glucose levels, but may be useful for detecting hyperglycaemia and hypoglycaemia.     

Neutrophil cell death, activation and bacterial infection in cystic fibrosis

BACKGROUND: Cystic fibrosis (CF) is characterised by chronic endobronchial bacterial infection and neutrophil mediated inflammation. Neutrophil apoptosis is essential for the resolution of inflammation. This study assessed the relationship between levels of neutrophil apoptosis and sputum microbiology in matched clinically stable patients with CF. METHODS: Sputum was induced from 34 patients (nine with no Gram negative infection, 10 colonised with Pseudomonas aeruginosa, 10 with Burkholderia cenocepacia, and five with other infections). Apoptotic neutrophils measured by flow cytometric Annexin V/propidium iodide staining and morphology were similar in all groups. RESULTS: Patients infected with P aeruginosa or B cenocepacia had a significantly lower percentage of viable neutrophils in the sputum than those with no Gram negative infection (Kruskal-Wallis p = 0.01, median (interquartile range (IQR)) 14.2% (9.4-21.6), 15.8% (12.3-19.5), and 48.4% (23.0-66.4); p = 0.003 and p = 0.002, respectively). They also had significantly higher levels of secondary necrotic granulocytes in sputum than patients with no Gram negative infection (Kruskal-Wallis p<0.0001, median (IQR) 55.5% (48.4-64.5), 50.4% (44.6-61.9), and 24.8% (14.4-30.5); p<0.0001 and p<0.0001, respectively). Neutrophils (x 10(6)/g sputum) in P aeruginosa infected patients (Kruskal-Wallis p = 0.05, median (IQR) 6.3 (3.5-12.7)) and B cenocepacia infected patients (5.7 (1.5-14.5)) were significantly higher than in the group with no Gram negative infection (0.5 (0.5-4.3), p = 0.03 and 0.04, respectively). CONCLUSION: These results suggest that cell death and clearance may be altered in patients with CF colonised with P aeruginosa and B cenocepacia compared with those with no Gram negative infection.     

Host defense mechanisms against influenza virus: interaction of influenza virus with murine macrophages in vitro.

The interaction of mouse macrophages with influenza virus was examined as part of a study into the defense mechanisms against influenza infection. Macrophages exposed to A/Port Chalmers/1/73 virus produced infectious foci on susceptible indicator cell monolayers. Sampling of supernatant fluids and cells from infected macrophage cultures showed release of virus adsorbed to the cell surface. Active virus replication in macrophages could not be demonstrated. Exposing macrophages to specific antibody before or after virus infection resulted in a significant decrease in the number of infectious macrophages. The results suggest that although macrophages are not the source of replicating influenza virus, they are able to spread the infection by having virus attaching to their surface. This activity is interfered with by the presence of specific antibody.     

Uroplakin III is not a major candidate gene for primary vesicoureteral reflux

Vesicoureteral reflux (VUR) is the retrograde flow of urine from the bladder into the ureter and towards the kidneys. VUR is the most common cause of end stage renal failure in both children and adults and it is a major cause of severe hypertension in children. VUR is seen in approximately 1-2% of newborn Caucasians. Substantial evidence exists that VUR is a genetic disorder. Uroplakins are integral membrane proteins found in the bladder wall. Knockout studies in mice have suggested uroplakin III (UPK3) as a candidate gene for VUR. We have used parametric and nonparametric linkage analysis and tests for association, to investigate this possibility in a cohort of 126 sibling pairs affected with primary VUR. None of the analyses showed any substantial evidence for linkage or association of markers at the UPK3 locus to VUR. Our results do not support a role for UPK3 in primary VUR.